As a selective estrogen receptor degrader in hormone replacement therapies, BZA demonstrates enhanced inhibitory potency against ERα mutants (Y537S and D538G) compared to tamoxifen and exhibits additional inhibitory activity in ER+ breast cancer cell lines when combined with the CDK4/6 inhibitor palbociclib [46] by inducing a G1 blockade in hormone-independent MCF-7:5C cells. The gene discussed is ESR1; the disease is breast carcinoma.